Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: TAL1 complex in human T-cell acute lymphoblastic leukemia (RPMI-8402)

PROVIDER: PRJNA170151 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR519112.fastq.gz	Fastqsanger.gz
	SRR519113.fastq.gz	Fastqsanger.gz
	SRR519114.fastq.gz	Fastqsanger.gz
	SRR519115.fastq.gz	Fastqsanger.gz
	SRR519116.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

TAL1 complex in human T-cell acute lymphoblastic leukemia (RPMI-8402)

2012-07-09 | GSE39179 | GEO

TAL1 complex in human T-cell acute lymphoblastic leukemia (RPMI-8402)

Project description:The oncogenic transcription factor TAL1/SCL is aberrantly overexpressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing the importance of the TAL1-regulated transcriptional program in the molecular pathogenesis of T-ALL. Here we identify regions occupied by TAL1 and its regulatory partners HEB, E2A, and GATA3 in a T-ALL cell line (RPMI-8402). Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total TAL1 (Santa Cruz SC-12984), TCF12/HEB (Santa Cruz SC-357),TCF3/E2A (Santa Cruz SC-349X), and GATA3 (Santa Cruz SC-22206).

2012-07-09 | E-GEOD-39179 | biostudies-arrayexpress

Core transcriptional regulatory circuit controlled by the TAL1 complex in human T-cell acute lymphoblastic leukemia

Project description:This SuperSeries is composed of the following subset Series: GSE29179: Identification of differentially expressed genes upon shRNA knockdown of TAL1 and its regulatory partners in T-ALL cells (Jurkat) GSE29180: ChIP-Seq of TAL1 and its regulatory partners in T-ALL cells (Jurkat) GSE33850: Core transcriptional regulatory circuit controlled by the tal1 complex in human t-cell acute lymphoblastic leukemia (Subseries) Refer to individual Series

2012-08-16 | E-GEOD-29181 | biostudies-arrayexpress

shRNA-mediated knockdown of Clock and Bmal1 genes in a T-cell acute lymphoblastic leukemia (T-ALL) cell line

Project description:Here, we report that the disruption of circadian clock obtained through shRNA-mediated knockdown of Clock and Bmal1 genes negatively impacted the in vitro growth of a T-cell acute lymphoblastic leukemia (T-ALL) cell line. We performed gene expression profiling analysis of RPMI-8402 cell line upon knock-down of the circadian genes Clock and Bmal1. We found that circadian clock directly infuences the expression of genes, such as IL20RB, involved in JAK/STAT signaling, making the T-ALL cells more responsive to Interleukin 20 (IL20).

2023-09-14 | GSE225005 | GEO

Genome wide maps of ZFX binding in human leukemia cell lines

Project description:Acute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) maintain the undifferentiated phenotype and proliferative capacity of their respective cells of origin, hematopoietic stem/progenitor cells and immature thymocytes. The mechanisms that maintain these progenitor-like characteristics are poorly understood. We report that transcription factor Zfx is required for the development and propagation of experimental AML caused by MLL-AF9 fusion, and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx activated progenitor-associated gene expression programs and prevented differentiation. Key Zfx target genes included mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescued the propagation of Zfx-deficient AML. These studies identify a common mechanism that controls the cell-of-origin characteristics of acute leukemias derived from disparate lineages and transformation mechanisms. Analysis of genomic ZFX binding in the AML cell line NOMO-1 and the T-ALL cell line RPMI-8402

2014-01-30 | E-GEOD-43147 | biostudies-arrayexpress

Homo sapiens

Project description:Core transcriptional regulatory circuit controlled by the tal1 complex in human t-cell acute lymphoblastic leukemia (Subseries)

| PRJNA148179 | ENA

An Oncogenic Super-Enhancer Formed through Somatic Mutation of a Noncoding Intergenic Element

Project description:In many cancers, critical oncogenes are driven from large regulatory elements, called super-enhancers, which recruit much of the cellM-bM-^@M-^Ys transcriptional apparatus and are defined by extensive H3K27 acetylation. We found that in T-cell acute lymphoblastic leukemia (T-ALL), somatic heterozygous mutations introduce MYB binding motifs in a precise noncoding site, which nucleate a super-enhancer upstream of the TAL1 oncogene. Further analysis of genome-wide binding identified MYB and its histone acetylase binding partner CBP as core components of the TAL1 complex and of the TAL1-mediated feed-forward auto-regulatory loop that drives T-ALL. Furthermore, MYB and CBP occupy endogenous MYB binding sites in the majority of super-enhancer sites found in T-ALL cells. Thus, our study reveals a new mechanism for the generation of super-enhancers in malignant cells involving the introduction of somatic indel mutations within non-coding sequences, which introduce aberrant binding sites for the MYB master transcription factor. ChIP-Seq for transcription factors and co-factors in T cell acute lymphoblastic leukemia cell lines

2014-11-13 | E-GEOD-59657 | biostudies-arrayexpress

Project description:Core transcriptional regulatory circuit controlled by the TAL1 complex in human T-cell acute lymphoblastic leukemia

| PRJNA139987 | ENA

Homo sapiens

Project description:PHF6 OCCUPANCYIN HUMAN T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA

| PRJNA196511 | ENA

Homo sapiens

Project description:UTX inhibition as selective epigenetic therapy against TAL1-driven T cell acute lymphoblastic leukemia

| PRJNA272133 | ENA